ReviewHeart failure clinics2026
The Pathogenic Role of the DNA Double-Stranded Breaks in Hereditary Cardiomyopathies.
Review in Heart failure clinics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Hereditary cardiomyopathies are caused primarily by mutations in genes encoding the protein constituents of cardiac myocytes. The mutation imparts biochemical, mechanical, and metabolic stresses, which not only induce the cardiomyopathy phenotype but also damage the nuclear and mitochondrial DNA, through oxidation, alkylation, cross-linking, and others. The DNA lesions, if unrepaired, cause replication and transcription stress, and activate the DNA damage response (DDR) pathways, which are composed of the repair, cell cycle checkpoint, and cytosolic DNA-sensing protein pathways. The DDR pathways provoke cell cycle arrest, instigate an interferon response, activate the nuclear factor Kappa B pathway. The induced gene expression causes inflammation, cell death, senescence, fibrosis, and organ dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.